The infection of HTLV-1 in patients with Strongyloides creates a unique imbalance of the immune responses resulting in increased susceptibility of host to disseminated disease.[11,30,31] It causes increased interferon-gamma (IFN-γ) production while decreasing levels of interleukin-4 (IL-4), IL-5, and IgE antibodies.[32–34] HTLV-1 can cause immunologic switching from Th-2 responses to Th-1 responses which favors hyperinfection. The gene discussed is IL5; the disease is infection.